γ-Aminobutyric acid （GABA） is the major inhibitory neurotransmitter in the central nervous system. The termination of GABA transmission is through the action of a family of membrane proteins, called GABA transporters （GAT1-4）. It is well established that GABA system is involved in the modulation of memory. Our previous study showed that homozygous GAT1^-/- mice exhibited impaired hippocampus-dependent learning and memory. To evaluate the impact of endogenous reduced GABA reuptake on mice cognitive behaviors, the ability of learning and memory of heterozygous GAT1^＋/- mice was detected by the passive avoidance paradigm and Morris water maze. The hole board paradigm was also used to measure changes in anxiety-related behavior or exploratory behav- ior in such mice. As one form of synaptic plasticity, long- term potentiation was recorded in the mouse hippocampal CA1 area. We found that GAT1^＋/- mice displayed increased learning and memory, decreased anxiety-like behaviors, and highest synaptic plasticity compared with wild-type and homozygous GAT1^-/- mice. Our results suggest that a moderate reduction in GAT1 activity causes the enhancement of learning and memory in mice.